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Study design Basic animal research. Objective The effects of granulocyte colony-stimulating factor (G-CSF) were assessed in a rat chronic spinal cord compression model to explore the potential of G-CSF as a pharmacological treatment for cervical spondylotic myelopathy. Summary of background data G-CSF is a hematopoietic cytokine used clinically to treat neutropenia. Recently, neuroprotective effects of G-CSF have been reported in spinal cord disorders. Methods To introduce the chronic cervical cord compression, thin polyurethane sheets were implanted under C5-C6 laminae of rats and gradually expanded by absorbing water. This model reproduces delayed compressive myelopathy of the cervical spine. In sham operations, the sheets were immediately removed. G-CSF (15 μg/kg) or normal saline (NS) was administered subcutaneously 5 days a week. Experimental groups were sham operation given NS; cord compression given NS; and cord compression given G-CSF. To assess motor functions, rotarod performance, and grip strength were measured. Twenty-six weeks after surgery, cervical spinal cords were examined histopathologically. In the prevention experiment, G-CSF or NS administration was started immediately after surgery. In the treatment experiment, their administration was started 8 weeks after surgery. In another experiment, in three groups in the prevention experiment, terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end labeling staining was performed to assess apoptotic cell death at 8 weeks after surgery. Results In the prevention experiment, administration of G-CSF preserved the motor functions and motor neurons throughout the 26 weeks, and significantly decreased the number of apoptotic cells at 8 weeks. In the treatment experiment, G-CSF administration from 8 weeks after surgery markedly restored the motor function temporarily to a level equal to the sham group. Conclusion G-CSF prevents the decline in motor functions and preserves motor neurons in the rat chronic cord compression model. G-CSF also improves motor function in the progressive phase of compression myelopathy. Level of evidence N/A.

Study design Sham-operation-controlled animal study to assess alterations in blood flow in the spinal cord in a chronic compression model. Laboratory investigation. Objective Cervical myelopathy is a common cause of disability in elderly patients. Hypothesis was made that ischemia subsequent to the spinal cord compression plays an important role in the pathogenesis of the spinal cord dysfunction. This study was undertaken to assess alterations in the blood flow of the spinal cord under chronic compression in a rat model. Summary of background data Histologic study of spinal cord from patients with spondylotic myelopathy showed ischemic tissue changes. Experimentally, spinal cord hypoperfusion in combination with chronic spinal cord compression induced myelopathy in dogs. We previously showed that chronic compression of the spinal cord in rats produces gradual deterioration of mobility of the animals accompanied by cord tissue degeneration compatible with ischemic changes. Methods Chronic compression of the cervical spinal cord was implemented by implantation of a thin urethane polymer sheet under the C5-C6 laminae, which expands by absorbing tissue water over 48-72 hours. The control group underwent sham operation. Twelve weeks later, blood flow to the C3-C4 and C5-C6 spinal cord segments were measured by fluorescent microsphere methods. Results In the control group, the blood flow in the C5-C6 segment was larger than C3-C4 segment. In the compression group, the blood flow in the C5-C6 was significantly reduced compared to the C3-C4 segment. Conclusion Under chronic focal spinal cord compression, there was a decrease of the blood flow in the compressed segment in comparison to the rostral segment. Our data are compatible with the hypothesis that alteration in the spinal cord blood flow contributes to pathogenesis of myelopathy.

OBJECTIVE AND IMPORTANCE Spinal accessory schwannomas unassociated with neurofibromatosis are very rare, and only 30 cases have been reported in the literature. To our knowledge, this is the first report of a spinal accessory schwannoma mimicking a tumor of the fourth ventricle. CLINICAL PRESENTATION A 50-year-old man presented with neck pain after being involved in a motor vehicle accident. There were no neurological deficits, but a computed tomographic scan revealed a large hypodense mass with punctuate calcifications in the fourth ventricle. The tumor exhibited low intensity on the T1-weighted magnetic resonance imaging scan and high intensity on the T2-weighted scan, and it showed inhomogeneous contrast enhancement. INTERVENTION The tumor was totally removed by a bilateral suboccipital craniectomy and C1 laminectomy. Dissection of the surgical specimen revealed that the tumor had originated from the left spinal accessory nerve. Histopathological examination confirmed the diagnosis of schwannoma. The patient experienced transient postoperative cerebellar ataxia but recovered completely. CONCLUSION Intracisternal-type spinal accessory schwannomas sometimes mimic a tumor of the fourth ventricle. Total surgical resection can be achieved with good outcome.

Scedosporium apiospermum, the asexual anamorph of Pseudallescheria boydii, is a ubiquitous saprophytic fungus that usually causes cutaneous/subcutaneous infection but may manifest as an invasive disease, often in immunocompromised hosts. Following an extensive literature review, we think that this case represents the first documented report of a primary infection of the spine in an immunocompetent patient. Despite extensive surgical debridement and itraconazole therapy, the patient died of multisystem organ failure of unknown etiology. Our case and three previously reported cases of P. boydii vertebral osteomyelitis highlight the importance of obtaining repeat cultures in patients with culture-negative vertebral osteomyelitis who fail to adequately respond to empiric standard antibacterial and/or antimycobacterial therapy. Combined surgical debridement and antifungal therapy have been required for eradication of P. boydii spinal infections in two previously reported immunocompromised patients, although the optimal antifungal regimen for this infection has not been established.